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Lp2通过TLR-4/MAPK/NFκB和Nrf2-HO-1/CYP2E1信号通路改善小鼠脂多糖诱导的肝损伤。

Lp2 improved LPS-induced liver injury through the TLR-4/MAPK/NFκB and Nrf2-HO-1/CYP2E1 pathways in mice.

作者信息

Chen Yiying, Guan Wuyang, Zhang Nan, Wang Yu, Tian Yuan, Sun Haiyue, Li Xia, Wang Yuhua, Liu Jingsheng

机构信息

College of Food Science and Engineering, Jilin Agricultural University, Changchun, China.

Jilin Province Innovation Center for Food Biological Manufacture, Jilin Agricultural University, Changchun, China.

出版信息

Food Nutr Res. 2022 Jul 5;66. doi: 10.29219/fnr.v66.5459. eCollection 2022.

DOI:10.29219/fnr.v66.5459
PMID:35903291
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9287763/
Abstract

BACKGROUND

Inflammatory liver diseases present a significant public health problem. Probiotics are a kind of living microorganisms, which can improve the balance of host intestinal flora, promote the proliferation of intestinal beneficial bacteria, inhibit the growth of harmful bacteria, improve immunity, reduce blood lipids and so on. Probiotics in fermented foods have attracted considerable attention lately as treatment options for liver injury.

OBJECTIVE

The aim of this study was selected probiotic strain with well probiotic properties from naturally fermented foods and investigated the underlying mechanisms of screened probiotic strain on lipopolysaccharide (LPS)-induced liver injury, which provided the theoretical foundation for the development of probiotics functional food.

DESIGN

The probiotic characteristics of Lp2 isolated from Chinese traditional fermented food were evaluated. Male KM mice were randomly assigned into three groups: normal chow (Control), LPS and LPS with Lp2. Lp2 were orally administered for 4 weeks before exposure to LPS. The liver injury of LPS-induced mice was observed through the evaluation of biochemical indexes, protein expression level and liver histopathology.

RESULTS AND DISCUSSIONS

After treatment for 4 weeks, Lp2 administration significantly reduced the LPS-induced liver coefficient and the levels of serum or liver aspartate transaminase (AST), alanine aminotransferase (ALT), tumor necrosis factor α (TNF-α), interleukin-6 (IL-6) and LPS, as well as decreasing the histological alterations and protein compared with the LPS group. Western-blotting results showed that Lp2 activated the signal pathway of TLR4/MAPK/NFκB/NRF2-HO-1/CYP2E1/Caspase-3 and regulated the expression of related proteins.

CONCLUSIONS

In summary, Lp2 suppressed the LPS-induced activation of inflammatory pathways, oxidative injury and apoptosis has the potential to be used to improve liver injury.

摘要

背景

炎症性肝病是一个重大的公共卫生问题。益生菌是一类活的微生物,可改善宿主肠道菌群平衡,促进肠道有益菌增殖,抑制有害菌生长,提高免疫力,降低血脂等。发酵食品中的益生菌作为肝损伤的治疗选择近来备受关注。

目的

本研究旨在从天然发酵食品中筛选出具有良好益生菌特性的菌株,并研究筛选出的益生菌株对脂多糖(LPS)诱导的肝损伤的潜在作用机制,为开发益生菌功能食品提供理论依据。

设计

对从中国传统发酵食品中分离出的Lp2的益生菌特性进行评估。雄性KM小鼠随机分为三组:正常饲料组(对照组)、LPS组和LPS加Lp2组。在暴露于LPS前4周口服Lp2。通过评估生化指标、蛋白质表达水平和肝脏组织病理学观察LPS诱导小鼠的肝损伤情况。

结果与讨论

治疗4周后,与LPS组相比,给予Lp2显著降低了LPS诱导的肝脏系数以及血清或肝脏中天冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)、肿瘤坏死因子α(TNF-α)、白细胞介素-6(IL-6)和LPS的水平,同时减少了组织学改变和蛋白质含量。蛋白质免疫印迹结果表明,Lp2激活了TLR4/MAPK/NFκB/NRF2-HO-1/CYP2E1/Caspase-3信号通路并调节相关蛋白的表达。

结论

综上所述,Lp2抑制LPS诱导的炎症通路激活、氧化损伤和细胞凋亡,具有改善肝损伤的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/247f/9287763/bbc835e4c9b2/FNR-66-5459-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/247f/9287763/fe308e1513b7/FNR-66-5459-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/247f/9287763/701cac597b75/FNR-66-5459-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/247f/9287763/4b7094cbbf4f/FNR-66-5459-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/247f/9287763/329b26d24e71/FNR-66-5459-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/247f/9287763/9dc22443fb83/FNR-66-5459-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/247f/9287763/b0b4df755043/FNR-66-5459-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/247f/9287763/bbc835e4c9b2/FNR-66-5459-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/247f/9287763/fe308e1513b7/FNR-66-5459-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/247f/9287763/701cac597b75/FNR-66-5459-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/247f/9287763/4b7094cbbf4f/FNR-66-5459-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/247f/9287763/329b26d24e71/FNR-66-5459-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/247f/9287763/9dc22443fb83/FNR-66-5459-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/247f/9287763/b0b4df755043/FNR-66-5459-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/247f/9287763/bbc835e4c9b2/FNR-66-5459-g007.jpg

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